ライフサイエンスコーパス: end organ

1 pe is a functionally distinct mechanosensory end organ.

2 that IFN-I may be acting at the level of the end-organ.

3 mmunity may be exercised at the level of the end-organ.

4 s, epithelial dilation with abnormal sensory end organs.

5 emically comparable to developing vestibular end organs.

6 and functional development of the vestibular end organs.

7 ensity were not found in the other inner ear end organs.

8 trajectories to innervate their appropriate end organs.

9 han the detection range of the corresponding end organs.

10 ithelia in the organ of Corti and vestibular end organs.

11 /auchene and zigzag, serve as mechanosensory end organs.

12 ying the diverse functions of cutaneous LTMR end organs.

13 forming units found in the blood and several end-organs.

14 The absence of consistent end organ abnormalities in many chronic pain syndromes h

15 in direction, suggesting differences in the end organ afferents activated by these two stimuli.

16 ion, which seeks to reduce the expression of end-organ allergic disease in children with established

17 eptibilities, adaptive immune responses, and end-organ alterations (particularly in airway mucous cel

18 eptibilities, adaptive immune responses, and end-organ alterations (particularly in airway mucous cel

19 thways, allowing better visualization of the end organs and peripheral nerves.

20 d by distinct combinations of mechanosensory end organs and the low-threshold mechanoreceptors (LTMRs

21 Adenoviruses (Ads) cause a wide array of end-organ and disseminated diseases in severely immunosu

22 al cardiovascular pathologies resides at the end organ, and is coupled to impairment of cyclic nucleo

23 patient's prognosis, hemodynamic stability, end organ, and neurologic status.

24 tion in PAD, novel techniques focused on the end-organ are needed to assess disease severity and meas

25 thelium of the organ of Corti and vestibular end organs as well as in cells of the spiral ganglion.

26 onment and the relative roles of pathway and end organ assessed by blocking the distal pathways to pr

27 I IFNs protect against both the humoral and end organ autoimmune syndrome of MRL/lpr mice, independe

28 Targeting the end-organ by inhibiting keratinocyte desmosome signaling

29 d direct metabolic injury of endothelial and end-organ cells contribute to vascular complications.

30 o 1.5 x 10(6)-fold) viral loads in blood and end organs compared to N13R10.

31 hronic, relentless disease in which delay of end-organ complications is the major treatment goal, GI

32 chromogranin A (CHGA) polymorphisms predict end-organ complications of hypertension, such as end-sta

33 iable clinical course, many patients develop end-organ complications that are associated with signifi

34 riate follow-up studies related to glycemia, end-organ complications, and graft function.

35 tential treatment for diabetic patients with end-organ complications.

36 wever, limited insight has been gained as to end-organ complications.

37 so-occlusive events drive the development of end-organ complications.

38 examined the development of their neural and end-organ components in wild-type and transgenic mice th

39 erogeneous population with varying levels of end-organ compromise, the development of specific, easil

40 results in worsening functional capacity and end-organ compromise.

41 en lipid accumulation was uncoupled from its end-organ consequences in IL-17RA(-/-) mice, which exhib

42 The CMR LGE may represent the end-organ consequences of sustained adrenergic activatio

43 The Merkel disc, a main type of tactile end organ consisting of Merkel cells (MCs) and Abeta-aff

44 Merkel discs are tactile end organs consisting of Merkel cells and Abeta-afferent

45 In this observational study, we assessed end organ damage and clinical symptoms with special focu

46 microL for more than 6 months are at risk of end organ damage and should be referred for specialized

47 is report suggest that EFE represents severe end organ damage associated with IVDA and portends poor

48 ecelerate the aging process as well as blunt end organ damage from obesity.

49 te that neutrophils are primary mediators of end organ damage in a novel humanized lupus mouse model,

50 er cell derangement in exacerbating postburn end organ damage in alcohol-exposed mice.

51 SDMA) predict and potentially contribute to end organ damage in cardiovascular diseases.

52 to induce erythrocyte sickling and eventual end organ damage in sickle cell disease (SCD).

53 ed by marked eosinophilia and progression to end organ damage in some, but not all, affected family m

54 rk of epithelial cell damage and can lead to end organ damage including renal failure.

55 receptor blocker on intermediate markers of end organ damage, and long-term end point trials are pla

56 ity, and of FCGR3A alleles as a biomarker of end organ damage, provide important insights into diseas

57 oimmunity should be considered distinct from end organ damage.

58 ed macrophages, neutrophils, and significant end organ damage.

59 ncreased salt sensitivity, inflammation, and end organ damage.

60 d spleen but were eliminated by 24 h without end organ damage.

61 oplasmacytic infiltration but no evidence of end-organ damage (anemia, constitutional symptoms, hyper

62 a significant improvement in SCD-associated end-organ damage (nephropathy, pulmonary hypertension, p

63 but often-beneficial effects in ameliorating end-organ damage and blood pressure elevation in experim

64 there was no association between DM without end-organ damage and BRVO (aHR, 0.92; CI, 0.81-1.04; P =

65 ned unexplained eosinophilia with associated end-organ damage and by a striking male predominance.

66 This observational study assessed end-organ damage and clinical symptoms during dose reduc

67 vidence that increased KCC activity worsened end-organ damage and diminished survival in sickle cell

68 ate and adaptive immune system contribute to end-organ damage and dysfunction in hypertension.

69 utcomes of adverse drug events can result in end-organ damage and even death.

70 ry is invoked as a mechanism contributing to end-organ damage and other complications of sickle cell

71 these cells may prove beneficial in reducing end-organ damage and preventing consequences of hyperten

72 lar protein deposition disease that leads to end-organ damage and related symptoms and requires a tis

73 of IL-2 to lupus-prone mice protects against end-organ damage and suppresses inflammation by dually l

74 reatable vascular risk factor, how it causes end-organ damage and vascular events is poorly understoo

75 sease severity was important; enrollees with end-organ damage caused by HTN had a 107% increased haza

76 viral system, thus preventing viral-mediated end-organ damage during the early stages of infection.

77 Both HTN and end-organ damage from DM contribute to arteriosclerosis,

78 2; CI, 0.81-1.04; P = 0.2), individuals with end-organ damage from DM had a 36% increased hazard of B

79 d with patients without DM, individuals with end-organ damage from DM have a heightened risk of CRVO,

80 Individuals with end-organ damage from hypertension (HTN) or diabetes mel

81 er of immune dysregulation, characterized by end-organ damage from lymphocytic infiltration and macro

82 0.002), and patients with DM complicated by end-organ damage had 52% lower odds of having KCN (adjus

83 The presence of hypertensive end-organ damage has been demonstrated in hypertensive c

84 onally, arterial hypertension and subsequent end-organ damage have been attributed to hemodynamic fac

85 Although secondary end-organ damage in diabetes has generally been thought

86 ression MIF alleles also are associated with end-organ damage in different autoimmune diseases.

87 er in attenuating this measure of myocardial end-organ damage in hypertensive patients with LV hypert

88 nsights on the genetics of susceptibility to end-organ damage in lupus glomerulonephritis have been d

89 vestigations must focus on the mechanisms of end-organ damage in model systems and how to translate t

90 ous system and promote T-cell activation and end-organ damage in peripheral tissues.

91 terial pathogens, but may also contribute to end-organ damage in sepsis.

92 rs of systemic intravascular coagulation and end-organ damage in septic mice.

93 he severity of BP elevation and hypertensive end-organ damage in several animal models.

94 , cause not only insulin resistance but also end-organ damage in the form of nonalcoholic fatty liver

95 tivation, subsequent T-cell infiltration and end-organ damage in the kidney in the development of hyp

96 nk to the high rates of death as a result of end-organ damage in the months after recovery from pneum

97 he association between aprotinin and serious end-organ damage indicates that continued use is not pru

98 nclusions are that, in most cases, patients' end-organ damage is expected to either stabilise or impr

99 rove evaluation techniques, and determine if end-organ damage is reversible with proper therapy.

100 ular signaling response that leads to target end-organ damage may be a more viable therapeutic strate

101 s, cardiovascular, hepatic, and reproductive end-organ damage or disease.

102 switching to IgG3 but have minimal effect on end-organ damage or survival in MRL/lpr mice.

103 countries with CVD or diabetes mellitus with end-organ damage receiving proven medications.

104 ssment for the presence of comorbidities and end-organ damage should be emphasized.

105 development of blood pressure elevation and end-organ damage that occur on delayed exposure to mild

106 row plasma cells, or both, in the absence of end-organ damage was used to define light-chain smoulder

107 ac arrest myocardial dysfunction, attenuated end-organ damage, and improved neurologic outcome and su

108 rombin is a powerful modifier of SCD-induced end-organ damage, and present a novel therapeutic target

109 icular (LV) hypertrophy, a marker of cardiac end-organ damage, is associated with an increased risk o

110 e renal disease, embolic events resulting in end-organ damage, renovascular complications, or hyperte

111 potential to promote high blood pressure and end-organ damage, we show here that angiotensin II cause

112 sis model in vivo to determine mortality and end-organ damage.

113 inically-relevant metabolic disturbances and end-organ damage.

114 uroretinal disorder as an indicator of other end-organ damage.

115 oduction and facilitating the development of end-organ damage.

116 otypes may protect from ensuing inflammatory end-organ damage.

117 to smaller distal arteries, causing ischemic end-organ damage.

118 tory and profibrotic cascades culminating in end-organ damage.

119 at IMT levels below thresholds for clinical end-organ damage.

120 pair, progressive fibrogenesis, and eventual end-organ damage.

121 NZB genes and induces significantly greater end-organ damage.

122 gens are neither required nor sufficient for end-organ damage.

123 en innate and adaptive immunity resulting in end-organ damage.

124 slow or prevent the development of diabetic end-organ damage.

125 ity and hypertension as well as hypertensive end-organ damage.

126 f primary bone marrow disease with secondary end-organ damage.

127 rteries, which leads to arteriosclerosis and end-organ damage.

128 d into a debilitating disorder with emerging end-organ damage.

129 sens systolic hypertension and its attendant end-organ damage.

130 The associated risks of hypoglycemia and end-organ diabetic complications remain.

131 egaly, intrarenal leukocyte trafficking, and end organ disease in a murine model of lupus.

132 approach for prevention of CMV syndrome and end organ disease.

133 oproliferation, autoantibody production, and end organ disease; animals doubly deficient for IFN-RI a

134 as an increased frequency of age-associated end-organ disease (e.g. cardiovascular complications, ca

135 of viral load correlate with development of end-organ disease and are moderated by pre-existing natu

136 tically significant improvements occurred in end-organ disease and were greater in patients with a co

137 Cytomegalovirus end-organ disease can be prevented by giving ganciclovir

138 te quantitative nucleic acid testing in some end-organ disease categories.

139 munity, but this may not suffice to engender end-organ disease in lupus.

140 These data indicate that end-organ disease in MRL/Fas(lpr) mice responds differen

141 t are key to the prevention and treatment of end-organ disease in this population and critical to the

142 However, their role in driving end-organ disease is less well understood.

143 wever, the direct contribution of T cells in end-organ disease like lupus glomerulonephritis (GN) is

144 with delayed development of viremia and CMV end-organ disease or death.

145 ve trait loci cluster' concept; hypertension end-organ disease quantitative trait loci are distinct f

146 BK virus (BKV) infection causing end-organ disease remains a formidable challenge to the

147 Early detection of CMV end-organ disease should help with treatment management.

148 the ability to provide transplants or other end-organ disease treatment, 3) cultural differences tha

149 subjects, 46 developed viremia, 14 developed end-organ disease, and 20 died.

150 ejection, allograft dysfunction, significant end-organ disease, and mortality.

151 disease, severe liver disease, diabetes with end-organ disease, chronic renal failure, and dementia)

152 of protection against cytomegalovirus (CMV) end-organ disease, CMV-specific interferon (IFN)- gamma

153 rug because of CMV antigen or DNA detection, end-organ disease, or any other cause.

154 phadenopathy, pathogenic autoantibodies, and end-organ disease-but surprisingly, reversion of autoimm

155 excess clotting on tissue function leads to end-organ disease.

156 g the development of inflammation-associated end-organ disease.

157 n systemic lupus erythematosus in context of end-organ disease.

158 for distinguishing patients at high risk for end-organ disease.

159 expression contributes to the development of end organ diseases such as HIV-1-associated CNS disease.

160 ld, likely due to 1) differences in rates of end-organ diseases, 2) economic differences in the abili

161 etic activation may contribute to, or worsen end-organ diseases, and reduce the possibility of ventri

162 lar disease, cancer, osteoporosis, and other end-organ diseases.

163 ally related to the premature onset of other end-organ diseases.

164 Thus, OS-dependent metabolic and end organ dysfunction of aging may result from life-long

165 End organ dysfunction, particularly liver and kidney, is

166 morbidities without a resulting increase in end organ dysfunction.

167 GVHD remain inadequate and commonly lead to end-organ dysfunction and opportunistic infection.

168 atory response to infection characterized by end-organ dysfunction distant from the primary site of i

169 poperfusion probably account for much of the end-organ dysfunction in African patients with severe se

170 n some instances, and the high prevalence of end-organ dysfunction that affects the pharmacokinetic a

171 strategy combining a code for infection and end-organ dysfunction was more sensitive in identifying

172 dices of global illness severity, markers of end-organ dysfunction, and profiles of hemodynamic insta

173 adverse events, time to death, occurrence of end-organ dysfunction, days of intensive care unit hospi

174 cate into the systemic circulation and cause end-organ dysfunction, including renal dysfunction.

175 ic leak was associated with the incidence of end-organ dysfunction, mortality, reoperation, and hospi

176 The main outcomes were 30-day mortality, end-organ dysfunction, reoperation, prolonged hospitaliz

177 requiring two ICD-9 codes for infection and end-organ dysfunction.

178 ge," may be a useful method to quantify the "end organ" effect of exposure to these various risks.

179 ure), lack of effect on regression of target end organ effects like left ventricular hypertrophy and

180 This global functionality explains how large end-organ effects can be induced through modest individu

181 Interestingly, the beneficial end-organ effects of candesartan in the nitric oxide syn

182 2 receptor genes expressed in the gustatory end organs enable bony vertebrates (Euteleostomi) to rec

183 scade activation, and fibrosis predict these end-organ events.

184 iltration are influenced by gender-dependent end-organ factors and may determine the progression of a

185 eficiency virus (HIV)-infected patients with end organ failure can safely receive an organ transplant

186 o 30 times as many people die as a result of end-organ failure than are fortunate enough to undergo t

187 advances in understanding the mechanisms of end-organ failure, and modulation of the inflammatory re

188 le midshipman use the saccule as the primary end organ for hearing to detect and locate "singing" mal

189 patterns of SCG connections, restoration of end organ function would be expected.

190 status, biomarkers, symptoms, hospital stay, end organ function, and mortality have all been employed

191 performance status < or = 2; and acceptable end organ function.

192 nucleotide variation in microRNAs can affect end-organ function and stress response.

193 scular disease risk factors and disorders of end-organ function have been reported.

194 diate both pancreatic beta-cell function and end-organ function offers the opportunity to develop the

195 Eligible patients had adequate end-organ function, an Eastern Cooperative Oncology Grou

196 1 (RECIST v1.1), adequate haematological and end-organ function, and no autoimmune disease or active

197 p performance status of 0 or 1, and adequate end-organ function.

198 al seed sequence modifies mRNA targeting and end-organ function.

199 factor-1 in injured tissue leads to improved end-organ function.

200 eviously treated solid tumours, and adequate end-organ function.

201 as occurred, treatment focuses on supporting end-organ function.

202 eria in Solid Tumors version 1.1, and normal end-organ function.

203 ECIST v1.1), and adequate haematological and end-organ function.

204 ia In Solid Tumors version 1.1, and adequate end-organ function.

205 r findings provide insights into how tactile end-organs function and have clinical implications for t

206 urgery outweigh the significant benefits for end-organ health.

207 Sex hormone dysregulation and altered end-organ hormone sensitivity might explain this organ-s

208 omplex, and hemodynamically diverse state of end-organ hypoperfusion that is frequently associated wi

209 thelin-1 (ET-1) on cholinergic mechanisms of end-organs (i.e. skin blood vessels and sweat glands) fo

210 e is made on the basis of factors other than end organ identity.

211 rves in invertebrates to complicated tactile end organs in mammals.

212 nical stimuli activate specialized cutaneous end organs in the bill, innervated by trigeminal afferen

213 te activation, and infection-mediated innate end-organ inflammation.

214 e euthanized and inflammatory responses, and end organ injuries were assessed.

215 ccumulation alone is not responsible for the end organ injury in cystinosis.

216 mbotic microangiopathy (TMA), and widespread end organ injury.

217 ex hormones have been shown to modulate some end-organ injury after shock, post-T/HS BM dysfunction h

218 may play an important role in sepsis-related end-organ injury and dysfunction, especially in the hear

219 ies, aGVHD diagnosis is typically made after end-organ injury and often requires invasive tests and t

220 erance to chromatin is the critical step for end-organ injury are discussed.

221 mics, decrease myocardial damage, and reduce end-organ injury from prolonged hypoperfusion.

222 in GCs and EF, are major contributors to the end-organ injury in systemic autoimmunity.

223 End-organ injury is evident, illustrated by the presence

224 Development of end-organ injury on ECMO and longer ECMO duration were a

225 ion and diagnosis of aHUS as the recovery of end-organ injury present appears to be related to the ti

226 and protected lupus-prone MRL/Lpr mice from end-organ injury.

227 to be high MIF producers develop accelerated end-organ injury.

228 ys, proinflammatory cytokine production, and end-organ injury.

229 nvolvement when compared to patients without end-organ involvement (P = 0.023, P = 0.005, and P = 0.0

230 by cold temperatures and that has different end-organ involvement and increased intracellular signal

231 as more than 1500 cells per microliter with end-organ involvement and no recognized secondary cause.

232 h those without DM (P = 0.45), patients with end-organ involvement from DM had a 27% increased hazard

233 y, risk of neurodevelopmental impairment and end-organ involvement with fungal infections in the neon

234 Because motion detected by the vestibular end organs is encoded in a head-fixed frame of reference

235 anglia are predetermined to innervate select end-organs is unknown.

236 brospinal fluid drainage (adjunct) to reduce end-organ ischemia.

237 ntimal destruction, arterial thrombosis, and end-organ ischemia.

238 rienced more neurological symptoms and other end-organ ischemic events than those without dissection.

239 yrinth of the oyster toadfish by using whole end organs labeled by immunofluorescence with monoclonal

240 erized by marked peripheral eosinophilia and end organ manifestations attributable to the eosinophili

241 a of 1.5 x 10(9)/L or higher and evidence of end organ manifestations attributable to the eosinophili

242 has resulted largely from therapies treating end-organ manifestations.

243 nstrated simultaneous entrainment of all CBR end-organ measurements, ranging from cardiac chronotropi

244 d in Ex16 rats, implicating both central and end-organ mechanisms in vagal enhancement.

245 d dehydrogenase type 1 (11betaHSD1) performs end-organ metabolism of glucocorticoids (GCs) by catalyz

246 ted therapeutics aimed at reducing the major end-organ morbidities of chronic SF.

247 tructive sleep apnea (OSA) leads to multiple end-organ morbidities that are mediated by the cumulativ

248 ntly present, is associated with substantial end-organ morbidities that primarily but not exclusively

249 impact of PAD upon microvascular flow in the end-organ, muscle, remains unknown.

250 demonstration of TH-ir terminals in the main end organ of hearing in a nonmammalian vertebrate sugges

251 ously an inaccessible, but highly important, end organ of the brain.

252 ferents from the sacculus, the main auditory end organ of the inner ear, to individual tones were mea

253 well as in the adrenal medulla (AM), a major end organ of the sympathetic nervous system.

254 The sensory end organs of the inner ear of the lungfish, Protopterus

255 eceptor cells of the auditory and vestibular end organs of vertebrates acquire various types of potas

256 h CGRP staining was absent in the vestibular end-organs of null (-/-) mice, cholinergic staining appe

257 utside the cardiac vasculature, resulting in end-organ optic nerve ischaemia.

258 inability to meet metabolic requirements of end organs or skeletal muscle.

259 rocedures is a major complication leading to end-organ or limb ischemia.

260 ion, hematological abnormalities, markers of end-organ or right ventricular dysfunction, and lack of

261 us nephritis (LN) is a potentially dangerous end organ pathology that affects upwards of 60% of lupus

262 n, pLVAD support was able to safely maintain end-organ perfusion despite extended periods of hemodyna

263 d skin sympathetic nerve activity (SSNA) and end-organ peripheral vascular responsiveness are unclear

264 suggests that the non-neuronal components of end organs play an active role in signaling to LTMRs and

265 t is CD39 deletion on NK cells that provides end-organ protection, which is comparable to that seen i

266 Volatile agents may possess important end-organ protective properties mediated via cytoprotect

267 hways directly connecting sensory neurons to end organs; recurrent and reciprocal connectivity among

268 End-organ repair by adult haemopoietic stem cells is und

269 nce to the development of cGN is mediated by end organ resistance to damage.

270 hat increases in activity do not result from end-organ resistance but rather from lowered urinary ATP

271 temic autoimmunity, end-organ responses, and end-organ resistance to damage are also critical in dete

272 lts from compromised ATP release rather than end-organ resistance: ENaC in Cx30(-/-) mice responds to

273 In addition, studies of end-organ responses provide new targets for therapeutic

274 e that in addition to systemic autoimmunity, end-organ responses, and end-organ resistance to damage

275 ed a significant and specific attenuation of end-organ responsiveness to CBR-mediated sympathoexcitat

276 ark of sepsis, resulted in underperfusion of end organs, resulting in their damage.

277 The CMV viral load determined with the end-organ sample, the BAL fluid sample, was higher than

278 hogenic role in the pernicious metabolic and end-organ sequelae of obesity.

279 noclonal gammopathy, immune suppression, and end-organ sequelae.

280 Efferents to the sacculus, the main auditory end organ, showed features especially well adapted for m

281 ons; (ii) patients with a positive biopsy in end organs, such as the lung or stomach; (iii) symptomat

282 does not ensure correct matching of axon and end organ, suggesting that pathway choice is made on the

283 nts such as the initial fluid resuscitation, end-organ support, pain management, nutrition support, a

284 autoreactive T cells and genetic control of end organ susceptibility.

285 oci will permit future genetic dissection of end-organ susceptibility in murine lupus.

286 d non-cardiac SNA baroreflex is also seen in end-organ sympathetic outflows (adrenal and renal nerves

287 rly neutrophil infiltrate, and protection of end-organ target pathology are different, depending on w

288 immune system may be important in generating end-organ targeting Abs, the extent of damage inflicted

289 role in both propagation of autoimmunity and end-organ targeting.

290 iology: how are signals processed in sensory end organs, taste buds?

291 To evaluate the end-organs, taste buds and a class of putative taste rec

292 Neurobiotin labeling of the main auditory end organ, the saccule, combined with tyrosine hydroxyla

293 tion not only in lymphoid organs but also in end organs, thereby preventing the break in tolerance.

294 Significantly, end-organ tissue injury was not significantly different

295 has let mammals develop complicated tactile end organs to enable sophisticated sensory tasks, includ

296 ransport of a lipophilic dye from peripheral end organs to the dorsal medulla shows that fibers from

297 ecent studies of immunosuppressive efficacy, end-organ toxicities, and side effects of nonspecific im

298 NO resistance, endothelial dysfunction, and end-organ vasculopathy.

299 levels may provide a potential biomarker for end-organ vulnerability.

300 ation of autoantibodies, which accumulate in end-organs where they induce disease.